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1.
籼稻品种窄叶青8号抗稻瘟病基因分析 总被引:15,自引:4,他引:11
籼稻品种窄叶青8号是我国北方稻区水稻育种上重要的稻瘟病抗源之一。本文利用我国北方稻区的代表菌系中10-8-14和日本的代表菌系研54-04,对窄叶青8号与感病品种京系17号和丽江新团黑谷的杂交F1F2、DH和B1F1群体进行抗病性鉴定,根据抗病性的分离,确认窄叶青8号的抗性由1对显性主效基因,即朱立煌等报道的Pi-zh基因控制。利用系研54-04接种窄叶青8号与9个具有已知抗病基因的鉴别品种杂交的F2群体,各群体都表现二基因的独立遗传,证明Pi-zh基因与Pi-i、Pi-km、Pi-z、Pi-ta、Pi-taz、Pi-zt、Pi-kp、Pi-b和Pi-t等9个已知抗病基因间存在非等位关系,是新的抗稻瘟病基因。 相似文献
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太湖流域粳稻地方品种黑壳子粳对稻瘟病抗性的遗传分析 总被引:6,自引:0,他引:6
太湖流域粳稻地方品种黑壳子粳对稻瘟病菌表现抗谱广,抗性强的特点,利用黑壳子粳与感病的云南稻地方品种丽江新团黑谷杂交获得的F1、F2和RIL群体,在苗期喷雾接种研54-04和北1两个日本稻瘟病鉴别菌系,根据抗感反应分析亲本的抗病基因组成,结果表明,黑壳子粳对菌系北1的抗性由一对显性基因控制,对菌系研54-04的抗性由两对互为独立遗传的显性基因控制,等位性测定结果和重组自交系的抗感反应表明:黑壳子粳对菌系北1的抗病基因兼抗菌系研54-04,该抗病基因与Pi-k,Pi-z,Pi-ta,Pi-b,Pi-t等5个已知抗病基因座呈非等位关系。也不是Pi-i和Pi-a基因,推断是一个未知的新基因;另一个抗病基因抗菌系研54-04,感菌系北1。 相似文献
3.
一个新的水稻迟熟性基因的遗传分析和分子标记定位 总被引:9,自引:1,他引:8
中籼迟熟水稻品系8987含未知的长生育期基因,在杂交水稻育种中有重要的利用价值,应用该品系与4个不同生态类型的水稻品种杂交,对其F1和F2群体进行生育期调查和遗传分析,确认8987的长生育期受1对隐性主效基因控制。以(8987X地谷)F2群体为基础,应用RFLP和微卫星标记结合群分法,发现第7染色体的RFLP标记C213与该基因连锁;进一步应用F2分离群体将该基因定位于第7染色体上,暂定名为lf-3。此基因的发现和定位将有助于分子标记辅助选择和杂交水稻的改良。 相似文献
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用PCR技术诊断水稻的白叶枯病抗性 总被引:23,自引:1,他引:22
植物育种中应用分子标记辅助选择要求分子标记与目的基因紧密连锁,而且分析手段经济简便、重复性好。Xa21是最近发现的一个具有广谱抗性的水稻白叶枯病抗性基因,利用一个含Xa21基因的品系IRBB21分别与2个感病品种杂交获得2个F_2群体。用4对引物分别对3个亲本进行PCR分析,其中一对引物(PB78)的PCR产物在抗、感病品种间可揭示多态性。对2个F_2群体进一步的遗传分析表明,PCR标记和Xa21的白叶枯病抗性紧密连锁,其重组率仅为2.48%。根据该标记选择基因型纯合的抗性植株,其准确率可达100%。本文还就植物育种中分子标记的检测途径进行了评价。 相似文献
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水稻细菌性条斑病和白叶枯病抗性遗传研究 总被引:7,自引:0,他引:7
分析了Hashikalmi,Dular和90IRBBN44三个抗源品种对水稻细菌性条斑病S-103菌株和白叶枯病P1菌系的抗性遗传。结果表明,Hashikalmi和Dular对S-103的抗性均由2对隐性基因所控制,90IRBBN44则带有1对隐性抗性基因。经等位性测定表明,Hashikalmi和Dular的2对基因中至少有1对是等位的,但它们与90IRBBN44的1对基因均不等位。3个抗源品种对P1的抗性都受1对隐性基因控制,该基因与xa-5等位。连锁遗传分析表明,Hashikalmi和Dular对S-103的2对抗细条病基因中的1对与xa-5相连锁,而90IRBBN44的1对抗性基因与xa-5呈独立遗传。本文还就开展水稻抗细菌性条斑病育种进行了讨论。 相似文献
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中间偃麦草与小麦杂种配子形成途径的细胞学研究 总被引:5,自引:0,他引:5
以中间偃麦草与小麦烟农在15的发杂种子F1及其5个自交和回交世代(F2,F3,BC1,BC2,BC3)为材料,对杂种F1配子形成途径的细胞学特点进行了研究。结果表明,杂种F1减数第一分裂基本正常,在减数第二分裂观察到由于当染色体不对称分离产生的无染色质和仅带有微核的子细胞,小孢子染色体数目为24~35条,根据BC1推算的F1产生的雌配子染色体数目为20~35条,F2根尖细胞和花粉母细胞内染色体数目 相似文献
10.
广谱抗病基因的利用是控制稻瘟病最有效和最经济的方法。来源于华南的地方稻种暹罗占对稻瘟病菌表现出广谱抗性,以普感品种丽江新团黑谷为轮回亲本选育的暹罗占近等基因系NIL-XLZ对测试的44个不同来源稻瘟病菌的抗性频率为84.4%,其抗谱优于广谱抗瘟基因Pi2、Piz,与抗瘟基因Pi9和Pi50相近。为进一步了解暹罗占抗稻瘟病的遗传基础,以感病品种广恢290为母本、暹罗占为父本,构建了广恢290/暹罗占的F2遗传分离群体。选取致病谱较广的稻瘟病菌代表菌株GD08-T19对来源于广恢290/暹罗占的F1与F2个体进行了抗病遗传分析,结果显示F1个体全表现抗病,1760个F2个体的抗感分离比率为4.06∶1,表明暹罗占至少含有一个显性的抗稻瘟病基因。利用分布于Pi2、Pi1、Pita座位附近的44对SSR引物,对构建的抗/感基因池及遗传分离个体进行了分析,将暹罗占含有的一个抗瘟基因定位于水稻第6染色体Pi2/Pi9/Pi50基因家族区域247 kb的范围内。抗菌谱分析、基因特异性分子标记检测及测序分析结果表明:暹罗占含有广谱抗瘟基因Pi50。本研究结果为暹罗占在水稻抗病育种上的应用提供了重要依据。 相似文献
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A B-lectin receptor kinase gene conferring rice blast resistance 总被引:58,自引:0,他引:58
Chen X Shang J Chen D Lei C Zou Y Zhai W Liu G Xu J Ling Z Cao G Ma B Wang Y Zhao X Li S Zhu L 《The Plant journal : for cell and molecular biology》2006,46(5):794-804
Rice blast, caused by the fungal pathogen Magnaporthe grisea, is one of the most devastating diseases in rice worldwide. The dominant resistance gene, Pi-d2 [previously named Pi-d(t)2], present in the rice variety Digu, confers gene-for-gene resistance to the Chinese blast strain, ZB15. Pi-d2 was previously mapped close to the centromere of chromosome 6. In this study, the Pi-d2 gene was isolated by a map-based cloning strategy. Pi-d2 encodes a receptor-like kinase protein with a predicted extracellular domain of a bulb-type mannose specific binding lectin (B-lectin) and an intracellular serine-threonine kinase domain. Pi-d2 is a single-copy gene that is constitutively expressed in the rice variety Digu. Transgenic plants carrying the Pi-d2 transgene confer race-specific resistance to the M. grisea strain, ZB15. The Pi-d2 protein is plasma membrane localized. A single amino acid difference at position 441 of Pi-d2 distinguishes resistant and susceptible alleles of rice blast resistance gene Pi-d2. Because of its novel extracellular domain, Pi-d2 represents a new class of plant resistance genes. 相似文献
12.
Identification of Two Blast Resistance Genes in a Rice Variety, Digu 总被引:10,自引:0,他引:10
X. W. Chen S. G. Li J. C. Xu W. X. Zhai Z. Z. Ling B. T. Ma Y. P. Wang W. M. Wang G. Cao Y. Q. Ma J. J. Shang X. F. Zhao K. D. Zhou L. H. Zhu 《Journal of Phytopathology》2004,152(2):77-85
Blast, caused by Magnaporthe grisea is one of most serious diseases of rice worldwide. A Chinese local rice variety, Digu, with durable blast resistance, is one of the important resources for rice breeding for resistance to blast (M. grisea) in China. The objectives of the current study were to assess the identity of the resistance genes in Digu and to determine the chromosomal location by molecular marker tagging. Two susceptible varieties to blast, Lijiangxintuanheigu (LTH) and Jiangnanxiangnuo (JNXN), a number of different varieties, each containing one blast resistance gene, Piks, Pia, Pik, Pi‐b, Pi‐kp, Pi‐ta2, Pi‐ta, Pi‐z, Pi‐i, Pi‐km, Pi‐zt, Pi‐t and Pi‐11, and the progeny populations from the crosses between Digu and each of these varieties were analysed with Chinese blast isolates. We found that the resistance of Digu to each of the two Chinese blast isolates, ZB13 and ZB15, were controlled by two single dominant genes, separately. The two genes are different from the known blast resistance genes and, therefore, designated as Pi‐d(t)1 and Pi‐d(t)2. By using bulked segregation method and molecular marker analysis in corresponding F2 populations, Pi‐d(t)1 was located on chromosome 2 with a distance of 1.2 and 10.6 cM to restriction fragment length polymorphism (RFLP) markers G1314A and G45, respectively. And Pi‐d(t)2 was located on chromosome 6 with a distance of 3.2 and 3.4 cM to simple sequence repeat markers RM527 and RM3, respectively. We also developed a novel strategy of resistance gene analogue (RGA) assay with uneven polymerase chain reaction (PCR) to further tag the two genes and successfully identified two RGA markers, SPO01 and SPO03, which were co‐segregated toPi‐d(t)1 and Pi‐d(t)2, respectively, in their corresponding F2 populations. These results provide essential information for further utilization of the Digu's blast resistance genes in rice disease resistance breeding and positional cloning of these genes. 相似文献
13.
本文用累积分布曲线法对东农 363及农东415两个粳稻品种进行了抗稻瘟遗传分析,结果表明东农363对Hokul菌株的抗性是由一对显性抗性基因控制的,东农415对Ken53-33菌株的抗性是由两对互补的显性基因控制的;对Ina72菌株的抗性是由两对显性基因控制的,其中一对控制高抗反应,另一对控制中抗反应。两个杂交组合的正反交分析结果表明,水稻对稻瘟病菌的抗性遗传是由细胞核控制的,细胞质在抗瘟遗传中的作用在本试验的测试品种中并没有表现出来。
Abstract:By means of cumulative distribution curve methods,two Japonica varieties Dongnong 363 and Dongnong 415 were analysed for the inheritance of blast resistance.The results showed that the resistance of Dongnong 363 variety to Hokul blast strain was controlled by one dominant gene.The resistance of Dongnong 415 to Ken53-33 strain was controlled by two complementary dominant genes,to Ina72 strain was controlled by two dominant genes,one dominated over the high-resistant and the other over the middle-resistant.Genetic analysis of F3 plants of two reciprocal crosses showed that the resistance to the rice blast disease was controlled by nuclear gene,no cytoplasmic effect was found in the tested varieties. 相似文献
14.
抗稻瘟病体细胞突变体的抗性遗传分析 总被引:2,自引:0,他引:2
以ZA_(15)和ZB_(11)等2个致病小种对6个抗稻瘟病体细胞突变体进行了抗性遗传分析。结果表明,86-S1、88-86、88-42和88-40等4个突变体对ZA_15、ZB_(11)小种的抗性分别由1个显性基因控制,同时这2个抗性基因还存在紧密的连锁关系。88-127和88-145对ZA_15的抗病性受2个重复显性基因控制;而对ZB_(11)的抗性则分别受2个互补显性基因和1个显性基因控制。等位性测定表明,86-S1、88-42和8B-86等3个突变体具有的抗性基因是等位的,可能是Pi-(?)或与之等位的抗性基因。 相似文献
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籼稻品种浙辐802抗瘟性遗传研究 总被引:7,自引:0,他引:7
通过与8个日本鉴别品种杂交和利用日本代表菌系研54-04及我国南方稻区菌系95-h接种鉴定,研究了籼稻品种浙辐802的抗性遗传。研究结果表明,该品种对菌系研54-04的抗性由 2对显性基因控制,对菌系 95-t2的抗性由 1对显性基因控制。基因等位性分析确认,浙辐802中抵抗95-t2的抗病基因与Pi-i基因等位,与Pi-a、Pi-sh、Pi-k、Pi-z、Pi-b、Pi-t、Pi-ta等已知基因位点为非等位关系;抵抗菌系研54-04,感染菌系95-t2的基因与Pi-i、Pi-k、Pi-b、 Pi-t 4个已知基因位点为非等位关系。对这个基因与其他已知基因的等位性进行了分析,认为它可能是1个未被命名的新基因。 相似文献
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冈46B(G46B)是水稻生产应用中的一个农艺性状十分优良的保持系,其主要的缺陷是稻瘟病抗性较弱,通过对地谷,BL-1,Pi-4号等三个分别含抗病基因Pi-d(t)^1、Pi-b、Pi-tα^2的稻瘟病抗性材料与G46B聚合杂交,并利用抗病基因连锁的分子标记对杂交后代进行辅助选择,在聚合杂交的F2代及B1C1代群体中共获得了15株含Pi-d(t)^1、Pi-b、Pi-tα^2等三个抗稻瘟病基因的材料,其可能的基因型分别为:三基因杂合体Pi-d(t)^1pi-d(t)^1,Pi-bpi-b/Pi-tα^2 pi-tα^2 4株,双基因杂合体10株,其中Pi-d(t)^1Pi-d(t)^1/Pi-bpi-b/Pi-tα^2pi-tα^2 6株,Pi-d(t)^1pi-d(t)^1/Pi-bpi-b/Pi-tα^2Pi-tα^2 3株,Pi-d(t)^1pi-d(t)^1,Pi-bPi-6,Pi-tα^2 pi-tα^2 1株,双基因纯合体Pi-d(t)^1Pi-d(t)^1/Pi-bpi-b/Pi-tα^2Pi-tα^2仅1株,这一研究结果为进一步改良G46B的稻瘟病抗性奠定了基础,同时这一研究结果表明利用分子标记可快速、有效地实现多个抗病基因的聚合,大大提高水稻抗病育种的效率。 相似文献
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以太湖流域粳稻地方品种薄稻、铁杆青、江南晚和缺儿糯等广谱、高抗稻瘟病为材料, 与高感稻瘟病品种苏御糯杂交, 获得杂交F1、F2 , 分别接种日本稻瘟病鉴别菌系北1和中国稻瘟病菌生理小种ZE3、ZG1, 根据P1、P2、F1和F2等不同世代植株的抗、感反应, 分析地方品种对不同稻瘟病菌生理小种(菌系)的抗性遗传机理。结果表明: 薄稻、铁杆青及缺儿糯对北1菌系的抗性均可能由一对显性基因控制, 江南晚对北1的抗性则可能由两对抑制基因互作控制; 铁杆青及缺儿糯对ZE3小种的抗性均可能由一对显性基因控制, 薄稻和江南晚对ZE3小种的抗性可能分别由两对显性基因和两对抑制基因互作控制; 铁杆青对ZG1小种的抗性可能是由一对显性主基因控制, 薄稻和江南晚对ZG1小种的抗性则可能由两对抑制基因互作控制。进一步将薄稻与12个日本稻瘟病菌鉴别品种杂交,用北1菌系接种不同组合的F1和F2 , 进行抗病基因的等位性测定。结果表明, 薄稻对北1菌系的抗性基因与12个鉴别品种所携带的已知抗稻瘟病基因是不等位, 将该基因暂定为Pi-bd1(t)。 相似文献
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Rice blast disease is one of the most devastating diseases of rice
(Oryza sativa L.) caused by the fungus Magnaporthe oryzae (M. oryzae), and
neck blast is the most destructive phase of this illness. The underlying molecular
mechanisms of rice blast resistance are not well known. Thus, we collected 150
rice varieties from different ecotypes in China and assessed the rice blast
resistances under the natural conditions that favoured disease development in
Jining, Shandong Province, China in 2017. Results showed that 92 (61.3%) and
58 (38.7%) rice varieties were resistant and susceptible to M. oryzae,
respectively. Among the 150 rice varieties screened for the presence of 13 major
blast resistance (R) genes against M. oryzae by using functional markers, 147
contained one to eight R genes. The relationship between R genes and disease
response was discussed by analysing the phenotype and genotype of functional
markers. The results showed that the rice blast resistance gene Pita was
significantly correlated with rice blast resistance. Our results provided a basis for
the further understanding of the distribution of 13 major R genes of rice blast in
the germplasm resources of the tested rice varieties, and were meaningful for rice
disease resistance breeding. 相似文献
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The durably resistant rice cultivar Digu activates defence gene expression before the full maturation of Magnaporthe oryzae appressorium 总被引:1,自引:0,他引:1 下载免费PDF全文
Weitao Li Ya Liu Jing Wang Min He Xiaogang Zhou Chao Yang Can Yuan Jichun Wang Mawsheng Chern Junjie Yin Weilan Chen Bingtian Ma Yuping Wang Peng Qin Shigui Li Pamela Ronald Xuewei Chen 《Molecular Plant Pathology》2016,17(3):354-368